Denervated Stomach as an Esophageal Substitute Recovers Intraluminal Acidity With Time

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Abstract
To determine whether the denervated stomach as an esophageal substitute recovers normal intraluminal acidity with time. Bilateral truncal vagotomy to the stomach as an esophageal substitute reduces both gastric acid production and antral motility, but a spontaneous motor recovery process takes place over years. Intraluminal gastric pH and bile were monitored during a 24-hour period 1 to 195 months after transthoracic elevation of the stomach as esophageal replacement in 91 and 76 patients, respectively. Nine patients underwent a second gastric pH monitoring after a 3-year period. The percentages of time that the gastric pH was less than 2 and bile absorbance exceeded 0.25 were calculated in reference to values from 25 healthy volunteers. Eighty-nine upper gastrointestinal endoscopies were performed in 83 patients. Patients were divided into three groups depending on length of follow-up: group 1, less than 1 year; group 2, 1 to 3 years; group 3, more than 3 years. The prevalence of a normal gastric pH profile was 32.3% in group 1, 81.5% in group 2, and 97.6% in group 3. The percentage of time that the gastric pH was less than 2 increased from group 1 (27.3%) to group 2 (56.1%) and group 3 (70.5%), parallel to an increase in the prevalence of cervical heartburn and esophagitis. The percentage of time that the gastric pH was less than 2 increased from 28.7% to 81.2% in the nine patients investigated twice. Exposure of the gastric mucosa to bile was 12.8% in patients with a high gastric pH profile versus 19.3% in those with normal acidity. In the esophageal remnant in six patients, Barrett’s metaplasia developed, intestinal (n = 2) or gastric (n = 4) in type. Early after vagotomy, intraluminal gastric acidity is reduced in two thirds of patients, but the stomach recovers a normal intraluminal pH profile with time, so that in more than one third of patients, disabling cervical heartburn and esophagitis develop. The potential for the development of Barrett’s metaplasia in the esophageal remnant brings into question the use of the stomach as an esophageal substitute in benign and early neoplastic disease.